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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Interleukin 23 receptor

IL23R, interleukin-23 receptor
The protein encoded by this gene is a subunit of the receptor for IL23A/IL23. This protein pairs with the receptor molecule IL12RB1/IL12Rbeta1, and both are required for IL23A signaling. This protein associates constitutively with Janus kinase 2 (JAK2), and also binds to transcription activator STAT3 in a ligand-dependent manner. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: IL-23, IL-17, IBD, NOD2, CD4
Papers using IL23R antibodies
Papers on IL23R
Interactions of the Immune System with Skin and Bone Tissue in Psoriatic Arthritis: A Comprehensive Review.
Maverakis et al., Sacramento, United States. In Clin Rev Allergy Immunol, Feb 2016
In addition, there are numerous other genetic susceptibility loci (LCE3, CARD14, NOS2, NFKBIA, PSMA6, ERAP1, TRAF3IP2, IL12RB2, IL23R, IL12B, TNIP1, TNFAIP3, TYK2) and geoepidemiologic factors that contribute to the wide variability seen in psoriasis.
Interleukin-23-Induced Transcription Factor Blimp-1 Promotes Pathogenicity of T Helper 17 Cells.
Cua et al., Palo Alto, United States. In Immunity, Jan 2016
Furthermore, genome-wide occupancy and overexpression studies in Th17 cells revealed that Blimp-1 co-localized with transcription factors RORγt, STAT-3, and p300 at the Il23r, Il17a/f, and Csf2 cytokine loci to enhance their expression.
[Abnormal expression of IL- 23/IL- 17 axis in peripheral blood of 45 patients with primary immune thrombocytopenia].
Wu et al., Suzhou, China. In Zhonghua Xue Ye Xue Za Zhi, Jan 2016
METHODS: The real-time quantitative reverse transcription-polymerase chain reaction(RT-PCR)was used to determine the expression of IL-23p19, p40, p35, IL-23R, IL-12Rβ1, IL-12Rβ2, IL-17A, IL-17F mRNA in the peripheral blood of 45 ITP patients and 30 healthy controls.
Sulfasalazine Treatment Suppresses the Formation of HLA-B27 Heavy Chain Homodimer in Patients with Ankylosing Spondylitis.
Lai et al., Taiwan. In Int J Mol Sci, Dec 2015
However, SSA treatment did not affect the levels of IL-23 and IL-23R mRNAs.
Association of IL-23R Polymorphisms (rs6682925, rs10889677, rs1884444) With Cancer Risk: A PRISMA-Compliant Meta-Analysis.
Dai et al., Xi'an, China. In Medicine (baltimore), Dec 2015
Although interleukin (IL)-23 receptor (IL-23R) plays an important role in the pathogenesis of multiple cancers, its association with cancer risk is inconsistent across different studies.
Microarray and whole-exome sequencing analysis of familial Behçet's disease patients.
Nojima et al., Suita, Japan. In Sci Rep, Dec 2015
We performed DNA microarray analysis of peripheral blood mononuclear cell (PBMC) mRNA from 41 Japanese BD patients and revealed elevated levels of interleukin (IL) 23 receptor (IL23R) mRNA in many BD patients.
ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation.
Powrie et al., Oxford, United Kingdom. In Elife, Dec 2015
Together these data identify the IL-23R/GM-CSF axis within ILC3 as a key control point in the accumulation of innate effector cells in the intestine and in the spatio-temporal dynamics of ILCs in the intestinal inflammatory response.
Genetics of inflammatory bowel disease from multifactorial to monogenic forms.
Tommasini et al., Trieste, Italy. In World J Gastroenterol, Dec 2015
Some IBD associated genes are involved in innate immunity, in the autophagy and in the inflammatory response such as NOD2, ATG16L1 and IL23R, while other are implicated in immune mediated disease (STAT3) and in susceptibility to mycobacterium infection (IL12B).
The immunogenetics of Behçet's disease: A comprehensive review.
Remmers et al., Bethesda, United States. In J Autoimmun, Nov 2015
Genome-wide association studies have identified associations with genome-wide significance (P < 5 × 10(-8)) in the IL23R-IL12RB2, IL10, STAT4, CCR1-CCR3, KLRC4, ERAP1, TNFAIP3, and FUT2 loci.
Interleukin-23-Independent IL-17 Production Regulates Intestinal Epithelial Permeability.
Cua et al., Palo Alto, United States. In Immunity, Nov 2015
We have demonstrated that after acute intestinal injury, IL-23R(+) γδ T cells in the colonic lamina propria were the primary producers of early, gut-protective IL-17A, and this production of IL-17A was IL-23 independent, leaving protective IL-17 intact in the absence of IL-23.
An IL-23R/IL-22 Circuit Regulates Epithelial Serum Amyloid A to Promote Local Effector Th17 Responses.
Littman et al., New York City, United States. In Cell, Nov 2015
RORγt(+) Th17 cells are important for mucosal defenses but also contribute to autoimmune disease.
Association analyses identify 38 susceptibility loci for inflammatory bowel disease and highlight shared genetic risk across populations.
IBD Genetics Consortium et al., Groningen, Netherlands. In Nat Genet, Sep 2015
Nevertheless, we observe genetic heterogeneity between divergent populations at several established risk loci driven by differences in allele frequency (NOD2) or effect size (TNFSF15 and ATG16L1) or a combination of these factors (IL23R and IRGM).
Heterogeneity of autoimmune diseases: pathophysiologic insights from genetics and implications for new therapies.
Feldman et al., New York City, United States. In Nat Med, Jul 2015
Here we discuss our current understanding of the shared pathways of autoimmunity, including the tumor necrosis factor (TNF), major histocompatibility complex (MHC), interleukin 23 receptor (IL23R) and protein tyrosine phosphatase non-receptor type 22 (PTPN22) pathways.
Association of Interleukin-23 receptor gene polymorphisms with susceptibility to Crohn's disease: A meta-analysis.
Liu et al., Chengdu, China. In Sci Rep, 2014
Studies investigating the association between Interleukin-23 receptor (IL-23R) gene polymorphisms and Crohn's disease (CD) report conflicting results.
Genetic Associations of Interleukin-related Genes with Graves' Ophthalmopathy: a Systematic Review and Meta-analysis.
Chen et al., Hong Kong, Hong Kong. In Sci Rep, 2014
No association with GO was detected for the other 7 genes (IL1B, IL1RA, IL4, IL6, IL12B, IL13 and IL23R).
Interactions between IL17A, IL23R, and STAT4 polymorphisms confer susceptibility to intestinal Behcet's disease in Korean population.
Cheon et al., Seoul, South Korea. In Life Sci, 2012
Our results indicate that the interaction of specific IL17A, IL23R, and STAT4 modulate susceptibility to intestinal Behcet's disease in the Korean population
Cutting edge: a variant of the IL-23R gene associated with inflammatory bowel disease induces loss of microRNA regulation and enhanced protein production.
Kraal et al., Amsterdam, Netherlands. In J Immunol, 2012
findings show the rs10889677 variant in the 3'-untranslated region of IL-23R gene displays enhanced levels of both mRNA and production of IL-23R; this can be attributed to loss of binding capacity for the microRNAs Let-7e and Let-7f by the variant allele
Role of ATG16L, NOD2 and IL23R in Crohn's disease pathogenesis.
Thanigachalam et al., Orlando, United States. In World J Gastroenterol, 2012
role of ATG16L, NOD2 and IL23R in Crohn's disease [review]
[Association of interleukin-23 receptor gene polymorphisms with susceptibility and phenotypes of inflammatory bowel diseases in Jiangsu Han population].
Shi et al., Nanjing, China. In Zhonghua Nei Ke Za Zhi, 2011
Polymorphisms in IL23R confer susceptibility to inflammatory bowel diseases in the Jiangsu Han population.
STAT1 hyperphosphorylation and defective IL12R/IL23R signaling underlie defective immunity in autosomal dominant chronic mucocutaneous candidiasis.
Netea et al., Nijmegen, Netherlands. In Plos One, 2010
Mutated STAT1 inhibits IL12R/IL-23R signaling, with hyperphosphorylation of STAT1 as the likely underlying molecular mechanism.
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